Right Ventricular Infarction

DEMOGRAPHICS Case Title: Right Ventricular Failure Associated With Right Ventricular Infarct. Patient Name: Raven Frederick. Scenario Name: Right Ventricular Failure. Simulation Developers: Martin P. Eason, MD, JD; Jake L. Drumm, Critical Care NRMT-P. Date of Development: January 2010. Appropriate for following learning groups: Faculty: CME. Residents: Postgraduate year (PGY) 1-4. Specialties: Family Medicine, Internal Medicine, Critical Care, and Emergency Medicine. Medical Students (yr): 3-4. Other: Paramedic First Responders. CURRICULAR INFORMATION Educational Rationale Isolated right ventricular infarcts secondary to occlusive right coronary artery lesions are uncommon. However, right ventricle (RV) infarcts complicate 30% to 50% of inferior wall infarctions and ∼10% of anterior wall infarctions caused by multivessel disease. Proximal right coronary artery lesions put more myocardium at risk and, in the absence of collateral circulation, may result in bradyarrhythmias, atrioventricular (AV) block, and RV failure. The hemodynamic consequences of RV failure will require management considerations that differ from those of left ventricular ischemia/infarction. Specifically, drugs that may aid in the resolution of left ventricular ischemia may actually be detrimental to patients with right ventricular infarction. Moreover, failure to recognize this entity and inappropriate treatment may lead to rapid deterioration of patients. Therefore, it is important that health care practitioners learn to recognize right ventricular infarction and failure and understand its management. This scenario is designed to teach learners to recognize the presentation of RV infarct with failure, its complications, and management of this clinical entity. Discussion of Scenario We have used this scenario ∼10 times and believe that it is an excellent educational tool. Our learners have included PGY 1 and PGY 2 internal medicine and family medicine residents. We have also used this scenario (albeit in a less rigid manner) on third-year medical students. The learners have expressed universal approval of this case and liked the fact that RV infarct and failure is a new simulation subject. Learning Objectives Learners will be assessed on the following Accreditation Council for Graduate Medical Education core competencies: medical knowledge, patient care, practice-based learning and improvement, interpersonal and communication skills, professionalism, and systems-based practice. Recognize the clinical presentation of right ventricular infarction. Understand the pathophysiology of right ventricular infarction and failure. Understand the hemodynamic effects of right ventricular infarction and failure. Understand the initial management steps for right ventricular infarction. Understand the role of echocardiography in the management of right infarction and failure. Understand how to use a transthoracic and transvenous pacemaker to control complete heart block. Guided Study Questions How often is inferior infarction associated with right ventricular infarction? What are the hemodynamic effects of right ventricular failure? How does ischemia of the sinoventricular and AV nodes affect cardiac rhythm? How does venodilation affect cardiac output in right ventricular failure? What drugs should be used cautiously in suspected right ventricular failure? What is the role of echocardiography in the management of right ventricular failure? What are the management goals in right ventricular failure? References Used Horan L, Flower N. Right ventricular infarction: specific requirements of management. Am Fam Physician 1999;60:1727-1734. Dima C, Pershad A, Coven D. Right ventricular infarction: treatment & medication; eMedicine. Available at: http://emedicine.medscape.com/article/157961-treatment.Accessed October 9, 2008. Antman, Anbe DT, Armstrong PW, et al; American College of Cardiology; American Heart Association; Canadian Cardiovascular Society. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction—executive summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to revise the 1999 guidelines for the management of patients with acute myocardial infarction). J Am Coll Cardiol 2004;44:671-719. Didactics Assessment Instruments Checklist Initial presentation Obtain history Perform focused physical examination Cardiac Vascular [pulse and jugular venous distention (JVD)] Pulmonary Abdominal Recognize myocardial ischemia Obtain vital signs Order telemetry Order electrocardiogram (ECG) Recognize inferior infarction Order right-sided ECG Recognize right ventricular infarction Order laboratories Complete blood count Chemistry panel Cardiac isoenzymes and troponin Order chest radiograph Recognize normal chest radiograph ECHO—assess RV, left ventricle (LV) wall dyskinesia/akinesis; septal wall involvement; tricuspid valve pathology Order aspirin Avoid beta blockers or calcium channel blockers Attempt to transfer to catheterization laboratory Consider fibrinolytic therapy along with contraindications (Caution: postinfarction ventricular wall rupture and ventricular septal defect) Hypotension Recognize hypotension Request echocardiography Request central venous monitoring [and/or pulmonary artery (PA) catheter] Treat with fluids Avoid vasodilators Treat with inotropes when hypotension worsens Bradycardia Recognize and manage bradycardia Recognize complete heart block Consider anticholinergic or chronotrope Consider pacing; if transvenous, consider AV sequential pacing (Optional) place pacer on patient or pacing PA catheter Ventricular fibrillation and cardiac arrest If arrest occurs, appropriate advanced cardiac life support protocol for ventricular tachycardia and then fibrillation PREPARATION Monitors RequiredTableOther Equipment RequiredTableSupporting Files (Chest X-ray, Echocardiogram, Assessment, Handouts, etc) Normal chest radiograph. Echo video showing (if available) RV wall dyskinesis/akinesis; septal wall motion. ECG showing inferior infarction (ST elevation II, III, and F). Right-sided ECG showing infarction ST elevation in leads RV3-RV6. Laboratory values for chemistry, troponin, and isoenzymes levels. Time DurationTableCase Stem A 64-year-old woman arrives at the emergency department with “indigestion” for 2 hours, described as a funny feeling in her back. She has had this before but never sought medical attention. Today, she also feels nauseated and lightheaded. She has a history of mild hypertension and “the sugar,” which she says she controls with “diet.” Background and Briefing Information for Facilitator/ Coordinator's Eyes Only This simulation deals with a patient who is experiencing a right ventricular infarction. Recognition of this event is important as the management differs from that of left ventricular infarction. The vital signs are designed to allow the learners to consider ordering nitroglycerine when presented with an acute coronary syndrome (ACS). Her heart rate (HR) is relatively slow for her degree of distress, suggesting potential problems with her SA node. Because she is diabetic, her presentation of coronary ischemia is atypical. The initial ECG (left sided) should lead the learner to consider ACS (Fig. 1; also available as Supplemental Digital Content 1, https://links.lww.com/SIH/A16). Because it shows inferior infarction, the learner should order the right-sided ECG to make the diagnosis of RV infarct before ordering nitrates. They will initially be given the left-sided ECG followed by the ECG showing the lateral right-sided lateral changes (but only if requested) (Fig. 2; also available as Supplemental Digital Content 2, https://links.lww.com/SIH/A17). Although the appropriate response when making the diagnosis is to transfer the patient to the catheterization laboratory, the purpose of this exercise is to help learners understand the complications and management of RV failure. Therefore, they will be informed (if they request transfer to the catheterization laboratory) that it will not be available for an hour. In addition, many learners fail to make diagnosis of RV infarct before ordering nitrates, and the scenario is designed to demonstrate the effects of increased venous compliance in RV failure. The scenario will progress to RV failure and bradycardic rhythm disturbances. The learners are also given the opportunity to consider invasive monitoring, cardiac pacing, and echocardiography to diagnose and guide management in resolving this scenario. Optionally, if the patient deteriorates, review of ACLS protocol is also part of this learning module. At various points, the scenario may be “accelerated” to reflect a more realistic timeline.Figure 1.: ECG showing inferior infarction (ST elevation II, III, and F).Figure 2.: Right-sided ECG showing infarction in lateral leads (ST elevation RV4).Right-sided infarctions primarily involve occlusion of the right coronary artery. It is frequently associated with inferior infarcts. Because of the coronary supply, ischemia may also affect the sinoventricular and AV node resulting in bradyarrhythmias. The more proximal lesions are associated with greater infarct size. Ischemia and injury to RV tissue lead to poor compliance and contractility of the RV and lead to RV failure. This in turn leads to decreased stroke volume. The optimal therapy for RV infarction is catheterization and early reperfusion. However, this is not always possible and understanding the clinical presentation of this entity and its management is important to learners who may have to manage its complications. Clinical findings include typical signs and symptoms of coronary ischemia but may also include those associated with hypotension. Practitioners should also be on guard for atypical presentations. A physical examination may reveal hypotension with clear lung fields and increased JVD. There may be evidence of tricuspid regurgitation. Diagnosis is made by obtaining a right-sided ECG and evaluating the lateral leads. Because inferior infarctions are frequently associated with right ventricular infarcts, it is recommended that a right-sided ECG be obtained in patients with evidence for inferior infarctions. Management of a RV infarct must take into consideration the pathophysiologic effects of RV dysfunction. Because decreases in venous return may severely affect RV preload, drugs that increase venous capacitance, such as nitroglycerine, should be used with caution as even small doses may severely decrease cardiac output by their effects of right ventricular preload. If there is evidence of decreased nodal dysfunction, drugs that slow nodal conduction should also be avoided (calcium channel blockers and beta blockers). If there is tachycardia, judicious use of small titrated doses of beta blockers may be used, as these may help improve oxygen supply demand balance. Management includes not only fluid management to maintain preload but also avoidance of overloading the RV so as not to affect left ventricular function. Too vigorous fluid administration may increase right ventricular end diastolic volume leading to the displacement of the septum resulting in the distortion of the LV. This may worsen cardiac output by affecting left ventricular stroke volume. Therefore, the clinician is left with the therapeutic dilemma of having to increase right ventricular pressures to maintain right-sided stroke volume while avoiding affecting left ventricular stroke volume. Echocardiography if available in the emergency department is useful in determining the presence and degree of right ventricular failure. If the patient shows poor RV function, a fluid challenge (may take up to 2 L) is recommended to treat hypotension. Clinical signs such as JVD may be used to guide volume administration. Central venous monitoring may be instituted and fluid administration be continued to achieve filling pressures of 15 mm Hg. Continued fluid administration in the face of high RV filling pressure may decrease LV preload by the effects of the septum bowing into the LV. If hypotension persists, consideration should be given to initiation of inotropic agents such as beta agonists or phosphodiesterase inhibitors (milrinone). Milrinone is useful because it will increase inotropy and because its effects on pulmonary arterial resistance may decrease RV afterload. Agents with alpha agonist properties should be used judiciously, as they may increase pulmonary resistance leading increased right ventricular afterload. Similarly, conditions that may increase pulmonary arterial pressures such as positive end-expiratory pressure, hypoxemia, and hypercarbia should be avoided. Optimizing cardiac output can also be obtained by maintaining normal HRs. Because this condition is often associated with bradyarrhythmias, treatment of bradycardia with atropine or pacing will improve cardiac output. If possible, maintaining AV synchrony with AV sequential pacing is preferred over RV pacing to take advantage of the increase in preload from atrial contribution. Because the RV can tolerate ischemia better than the left (less oxygen demand, better collateral circulation, and coronary perfusion occurs in both diastole and systole), early reperfusion results in significantly preserved function. The purpose of this exercise is for the participants to recognize the presentation of a right ventricular infarct. They will be presented with a patient who appears to have an atypical ACS. Although they should consider percutanious coronary intervention and fibrinolytic therapy, the catheterization will not be available, and there will be a contraindication to fibrinolysis. If the learners order fibrinolytics, they will not be ready before the hypotension and bradycardia events occur. The challenges for the participants are as follows: Recognition of an RV infarct and potential RV failure. Management of hypotension in an RV infarct. Recognition of bradyarrhythmia and its management. Definitive treatment of an RV infarct. The sequence of the scenario will be as follows: Clinical presentation of ACS. Hypotension from, RV failure. Bradycardia and heart block. The participants may treat either problem simultaneously or sequentially. Debriefing Points Clinical presentation of right ventricular infarctions. Association with inferior infarcts. Right-sided ECG findings. Pathophysiology and complications of RV infarct. Blood supply. RV failure. Bradyarrthymias. Management of RV infarct. Avoidance of vasodilators. Diagnostic and monitoring modalities. Aggressive fluid administration. Inotropes. Treatment of bradyarrthymias with pacing. Early reperfusion. Other points depending on participant actions (eg, ACLS protocol). Procedural. How to use a transthoracic pacemaker. How to place and use a pacing PA catheter. PATIENT DATA BACKGROUND AND BASELINE STATE Patient History Review of Systems Central nervous system: within normal limits. Cardiovascular: hypertension, blood pressure (BP) normally runs 140/80, and hyperlipidemia. Pulmonary: no pulmonary problems. Renal/hepatic: none. Endocrine: type 2 diabetes mellitus. Hematology/coagulation: none. Gastrointestinal: peptic ulcer disease; had guaiac positive stools 3 weeks ago. Current Medications and Allergies Lisinopril, omeprazole, and glyburide Allergy: shellfish. Social History Smokes one pack of cigarettes per day. Physical Examination General: alert patient in mild distress. Weight and height: 65 inches and 85 kg. Vital signs: BP, 100/61; HR, 68; respiratory rate (RR), 24; oxygen saturation, 96%; and temperature, 37°C. Lungs: clear bilaterally to auscultation. Heart: S1 and S2 normal regular rate and rhythm. Telemetry if requested: shows sinus rhythm at rate of 68 with ST segment elevation in lead II. Laboratory, Radiology, and Other Relevant Studies White blood cells: 8200/mm3. Hematocrit: 42%. Hemoglobin: 125 g/L. Platelet count: 235,000/ mm3. Chemistry: sodium, 142 mEq (mmol/L); potassium, 4.1 mEq (mmol/L); chloride, 101 mEq (mmol/L); blood urea nitrogen, 12 mg/dL (4.9 mmol/L); creatinine, 1.2 mg/dL (106 mcmol/L); glucose, 175 mg/dL (9.1 mmol/L). Troponin I, <0.2 ng/mL (<0.2 mcg/L); troponin T, <0.1 mcg/L. Chest radiograph: normal chest. EKG: left sided ECG shows ST elevation in leads II, III, and F and ST segment depression in AVL (Figs. 1 and 2). If requested, right-sided ECG shows ST segment elevation in V4-6. Baseline Simulator State Vitals: BP, 105/61; HR, 68; respiratory rate, 24; and saturation 96% (Table 1).TABLE 1: Student Learning Outcomes or Actions Desired and Trigger to Move to Next StateTABLE 1: (Continued)TABLE 1: (Continued)Neuro: awake alert in mild distress. Respiratory: lungs are clear. Cardiovascular: rate is regular with no adventitious sounds. Gastrointestinal: normal bowel sounds. Genitourinary: N/A. Metabolic: N/A. Environmental.

Récupéré en direct depuis OpenAlex et désinversé. Les résumés ne sont pas conservés dans cette base de données : les index inversés représentent 8,6 Go des 9,3 Go de texte de la base, et le serveur dispose de 13 Go libres.